Renal 2- acute kidney injury and nephritic/ nephrotic syndrome Flashcards

1
Q

Definition of AKI

A

A rapid (within hours to days) fall in glomerular filtration rate which impedes the kidney’s normal functions

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2
Q

AKI stage 1

A

Increase in serum cratinine of 26 micromol/ litre or more within 48 hours

OR

1.5-2x increase from baseline

Less than 0.5ml/kg/hour for more than 6 hours

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3
Q

AKI stage 2

A

Increase in serum creatinine to more than 2-3x from baseline

Less than 0.5ml/kg/hour for more than 12 hours

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4
Q

AKI stage 3

A

Increase in serum creatinine to more than 3x from baseline

OR

Serum creatinine more than 354 micromol/litre with an acute increase of at least 44 micromol/litre

Less than 0.3ml/kg/hour for 24 hours or anuria for 12 hours

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5
Q

What is creatinine?

A

A normal product of muscle turnover

Non-toxic

Transported by the blood and excreted by the kidneys

Used as a surrogate marker for glomerular filtration

Less filtration -> less creatinine removed -> a creatinine rise

GFR is estimated from creatinine results

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6
Q

Normal range of creatinie

A

In Brighton 60-100 micromols/litre

What is normal for one patient may not be for another

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7
Q

Oliguria

A

<0.5ml/kg/hour urine output

Usually <500ml/ 24 hours in adults

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8
Q

Anuria

A

Officially would mean no urine output

Softly defined as <100ml/ 24 hours

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9
Q

Four phases of AKI

A

Onset phase

Oliguric/ anuric phase

Polyuric/ diuretic phase

Recovery phase

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10
Q

Onset phase- hours to days

A

Common triggering events

  • significant blood loss
  • burns
  • fluid loss
  • diabetes insipidus

Renal blood flow 25% of normal

Tissue oxygenation 35% pf normal

Urine output below 0.5ml/kg/hour

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11
Q

Oliguric/ anuric phase- 8-14 days or longer depending on nature of AKI

A

Urine output below 400ml/day, possibly as low as 100ml/day

Increase in BUN and creatinine levels

Electrolyte disturbances, acidosis and fluid overload (from kidney’s inability to excrete water)

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12
Q

Diuretic phase- 7-14 days

A

Occurs when AKI is corrected

Renal tubule scarring and oedema

Increased GFR

Daily urine output above 400ml

Possible electrolyte depletion from excretion of more water and osmotic effects of high BUN

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13
Q

Recovery phase- several months to 1 year

A

Decreased oedema

Normalisation of fluid and electrolyte balance

Return of GFR to 70% or 80% of normal

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14
Q

Kidney functions

A

Excretion of toxins

Electrolyte balance

Acid base balance

Fluid balance

NP control

Control of bone metabolism, vit D activation, phosphate excretion

Production of erythropoietin

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15
Q

Hyperkalaemia

A

K+ >6.0 = bad

K+ >6.5 = medical emergency

ECG

  • reduced P wave with widened QRS
  • tented T waves
  • sine wave pattern
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16
Q

Fluid overload

A

Symptoms

  • breathlessness
  • orthopnoea
  • limb swelling

The danger- pulmonary oedema- severe tissue hypoxia

If patient is oliguric/ anuric they won’t be able to get rid of excess water

17
Q

When to think about dialysis

A
  1. Refractory hyperkalaemia
  2. Pulmonary oedema
  3. Refractory acid/ base disturbance
  4. Uraemic complications (coma, pericarditis)
18
Q

What causes AKI?

A
  1. Pre-renal causes
  2. Renal causes
  3. Post-renal causes
19
Q

Pre-renal causes

A

Decrease in perfusion pressure resulting in ischaemia or infarction

  • bleeding
  • septic shock
  • dehydration
  • myocardial infarction
  • iatrogenic
  • renal artery stenosis

VERY LIKELY

20
Q

Renal causes

A

Direct toxic effects

  • drugs
  • calcium and other metals

Overproduction leading to blockage of the tubules

  • rhabdomyolysis
  • myeloma

Inflammation in the kidney

  • GN
  • interstitial nephritis
  • ATN

UNLIKELY

21
Q

Post renal causes

A

Plumbing problem/ outflow obstruction

  • stones
  • ureteric/ urethral strictures
  • BPH
  • prostate cancer
  • urinary retention e.g. neurogenic, constipation

Relatively LIKELY

22
Q

Who is at risk of AKI?

A

Chronic background risk:

  • elderly
  • CKD
  • cardiac failure
  • liver disease
  • diabetes
  • vascular disease
  • background nephrotoxic medications

Acute risk:

  • S: sepsis and hypoperfusion
  • T: toxins
  • O: obstruction
  • P: parenchyma
23
Q

Predict/ prevent AKI- the 4 Ms

A

Monitor
- obs/NEWS, regular blood tests, fluid balance charts, pathology alerts

Maintain circulation
- hydration, resuscitation, oxygenation

Minimise kidney insults
- nephrotoxic meds, surgery, contrast, hospital acquired infection

Mange the acute illness
- sepsis, heart failure, liver failure

24
Q

Treatment of AKI

A

Make the patient safe

  • ABCDE
  • what is K+
  • what is volume status

If hypovolaemic give 250/500ml bolus of saline

Monitoring

  • check catheter
  • strict fluid inputs/ outputs
  • check VBG

Investigate the cause once stable

25
Q

Red flags in history

A

Haemoptysis

Rashes

Joint pain/ swelling

ENT- crusting of nose/ acute hearing impairment

Significant acute limb swelling

Noticeable urine frothiness

Jaundice

26
Q

Drugs to hold in AKI

A

ACE inhibitors

Angiotensin receptor blockers

NSAIDS: ibuprofen, diclofenac, naproxen

Any diuretics

Metformin

27
Q

Causes of polyuria

A

Known and common phase of AKI of any cause

Post relief of obstruction

Diabetes mellitus

Psychogenic

Beer potomania

Rare endocrine causes (e.g. diabetes insipidus)

28
Q

Managing polyuria

A

Encourage the patient to drink

Depending on your assessment of fluid balance

  • provide IV fluids to match the output +/- additional input if dry
  • once renal function begins to improve reduce to 75% of urine output
29
Q

Managing oliguria

A

Depending on your assessment of fluid balance

If you have given 2-3 litres and can’t see blood on the floor ask for help